Log in

Relevant bibliographies by topics / Adipocyte

Contents

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers
Reports

Academic literature on the topic 'Adipocyte'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Adipocyte.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Adipocyte"

1

Thomalla, Miriam, Andreas Schmid, Julia Hehner, Sebastian Koehler, Elena Neumann, Ulf Müller-Ladner, Andreas Schäffler, and Thomas Karrasch. "Toll-like Receptor 7 (TLR7) Is Expressed in Adipocytes and the Pharmacological TLR7 Agonist Imiquimod and Adipocyte-Derived Cell-Free Nucleic Acids (cfDNA) Regulate Adipocyte Function." International Journal of Molecular Sciences 23, no. 15 (July 30, 2022): 8475. http://dx.doi.org/10.3390/ijms23158475.

Full text

Abstract:

Endosome-localized Toll-like receptors (TLRs) 3 and 9 are expressed and functionally active in adipocytes. The functionality and role of TLR7 in adipocyte biology and innate immunity of adipose tissue (AT) is poorly characterized. We analyzed TLR7 mRNA and protein expression in murine 3T3-L1 and primary adipocytes, in co-cultures of 3T3-L1 adipocytes with murine J774A.1 monocytes and in human AT. The effects of TLR7 agonists imiquimod (IMQ) and cell-free nucleic acids (cfDNA) on adipokine concentration in cell-culture supernatants and gene expression profile were investigated. We found that TLR7 expression is strongly induced during adipocyte differentiation. TLR7 gene expression in adipocytes and AT stroma-vascular cells (SVC) seems to be independent of TLR9. IMQ downregulates resistin concentration in adipocyte cell-culture supernatants and modulates gene expression of glucose transporter Glut4. Adipocyte-derived cfDNA reduces adiponectin and resistin in cell-culture supernatants and potentially inhibits Glut4 gene expression. The responsiveness of 3T3-L1 adipocytes to imiquimod is preserved in co-culture with J774A.1 monocytes. Obesity-related, adipocyte-derived cfDNA engages adipocytic pattern recognition receptors (PRRs), modulating AT immune and metabolic homeostasis during adipose inflammation.

APA, Harvard, Vancouver, ISO, and other styles

2

Jin, Linhua, Marina Konopleva, Yixin Zhou, Akimichi Osaka, Michael Andreeff, Takashi Miida, and Yoko Tabe. "Pro-Apoptotic and Proliferative Effects of Bone Marrow Adipocytes on Myeloid Leukemia Cells." Blood 114, no. 22 (November 20, 2009): 4572. http://dx.doi.org/10.1182/blood.v114.22.4572.4572.

Full text

Abstract:

Abstract Abstract 4572 Bone marrow stromal cells (MSCs) from elderly subjects have a reduced capacity to differentiate into osteoblasts and an increased capacity to differentiate into adipocytes, which leads to progressive accumulation of fat in the bone marrow space with increasing age. Adipocytes are the prevalent stromal cell type in adult BM that play an important role in the leukemic bone marrow microenvironment (Tabe et al., Blood 2004 103:1815-22). In this study, we examined the role of BM-derived adipocytes at different stages of differentiation on proliferation and apoptosis of AML cells. U937 cells were co-cultured with BM-derived MSC, MSC-differentiated pre-adipocytes (containing few small lipid vesicles), and mature adipocytes (with multiple hypertrophic lipid vesicules). Under serum-starved conditions, MSC and premature/mature adipocytes induced cell cycle progression of U937 cells with increase in the proportion of cells in S- and G2/M-phase fractions, and inhibited spontaneous cell death with decrease in subG1 fractions. However, only pre-adipocytes inhibited Ara-C-induced cell killing (Table 1). We next focused on lepin and plasminogen activator inhibitor 1(PAI-1) as potential mediators of these effects by adipocytes. Leptin mRNA and protein levels were upregulated during adipocytic differentiation (mRNA relative expression to GAPDH (PCR): MSC 0, premature adipocyte 2.0±0.5, mature adipocyte 123.3± 35.0; leptin secretion: MSC 23.1±2.9, premature adipocyte 49.3±11.3, mature adipocyte 110.0±4.6 pg/mL (ELISA). PAI-1 mRNA levels were increased in mature adipocyte (relative expression to GAPDH: MSC 314.9±46.5, premature adipocyte 215.1, mature adipocyte 3766.1±656.2). Since PPARÿ activation is known to promote maturation and re-generation of fat-derived adipocytes, we next examined the potential of the synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) on the BM adipocytes, leptin and PAI-1 production and the survival of the leukemic cells. CDDO induced adipocyte re-generation with significant increase of the number of Oil-Red(+) small sized lipid vesicles without apoptosis induction. This resulted in a markedly enhanced leptin release from adipocytes (10-fold and 23-fold increase at 0.5 μM and 1.0 μM CDDO, respectively, at 72 hrs) without change in leptin mRNA transcription. On the contrary, PAI-1 mRNA levels were significantly decreased by CDDO (6 fold decrease in MSC, 4 fold decrease in premature adipocyte, 6 fold decrease in mature adipocyte). Co-culture of U937 cells with CDDO-primed premature adipocytes and mature adipocytes resulted in increased spontaneous apoptosis of U937 cells compared to adipocytes not exposed to CDDO (% specific apoptosis, U937 co-cultured with CDDO-primed premature adipocytes 26.9 %, mature adipocytes 20.9 %). At the same time, CDDO-primed premature adipocytes induced significant cell cycle progression with decreased proportion of G0/G1-phase and increase in S-phase fractions in U937 cells (Table 2). Co-culture with CDDO-primed premature adipocytes or with premature adipocytes co-treated with recombinant leptin increased subG1- and S-phase fractions in Ara-C-treated U937 cells compared to U937 cells co-cultured with premature adipocytes (Table 3). In mature adipocytes, which already produce high levels of leptin, CDDO or leptin treatment failed to modulate anti-apoptotic or proliferative effects of AraC on U937 cells. In contrast, human recombinant PAI-1 effectively inhibited spontaneous and Ara-C induced apoptosis of U937 cells (decreased % of Annexin V: spontaneous apoptosis 11.2±1.1%, Ara-C induced apoptosis 15.1± 1.7%). In summary, these results suggest that BM pre-adipocytes support proliferation and survival of myeloid leukemia cells in part through complementary effects of leptin and PAI-1. Our findings indicate that secretion of leptin during MSC differentiation or through PPARg ligation promotes cell cycle progression, while PAI-1 primarily inhibits apoptosis of AML cells. It is conceivable that increased adipocyte content of BM in elderly AML patients may negatively affect the responsiveness of AML cells to chemotherapy. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

3

Naveiras, Olaia, Valentina Nardi, and George Q. Daley. "Bone Marrow Adipocytes Prevent Hematopoietic Expansion in Homeostasis and in Bone Marrow Transplantation." Blood 112, no. 11 (November 16, 2008): 551. http://dx.doi.org/10.1182/blood.v112.11.551.551.

Full text

Abstract:

Abstract In mammalian bone marrow (BM), osteoblasts and endothelium constitute functional niches that support hematopoietic stem cells (HSC). Adult BM also contains numerous adipocytes, whose numbers correlate inversely with the hematopoietic activity of the marrow. As described by Neumann’s law in 1882, distal skeletal regions are adipocytic and thus non-hematopoietic in the adult. Fatty infiltration of the hematopoietic red marrow also occurs following irradiation or chemotherapy and is a diagnostic feature in biopsies from patients with marrow aplasia. However, whether adipocytes participate in hematopoietic regulation or simply expand to fill marrow space is unclear. We have found that murine hematopoiesis is reduced in adipocyte-rich marrow during homeostasis, and that adipocytes antagonize marrow recovery post-irradiation. By flow cytometry, colony forming assay, and competitive repopulation, we found a reduced frequency of HSCs and short-term hematopoietic progenitors in the adipocyte-rich vertebrae of the tail compared to the adipocyte-free vertebrae of the thorax. In A-ZIP/F1 “fatless” mice, which are genetically incapable of forming adipocytes, post-irradiation marrow engraftment is accelerated relative to wild type mice. Likewise, pharmacologic inhibition of adipocyte formation with the PPARg inhibitor Bisphenol-A-DiGlycidyl-Ether (BADGE) enhances hematopoietic recovery after BM transplant. Moreover, we have found that mice deficient in the adipocyte-specific protein adiponectin, which has been described to inhibit hematopoietic progenitor expansion in vitro, have increased progenitors in fatty marrow both during homeostasis and after BM transplant. Our data implicate adipocytes as negative regulators of the bone marrow microenvironment, and demonstrate that antagonizing adipogenesis is advantageous for enhancing hematopoietic recovery in the setting of bone marrow transplantation.

APA, Harvard, Vancouver, ISO, and other styles

4

Smith, Jessica, Maha Al-Amri, Prabhakaran Dorairaj, and Allan Sniderman. "The adipocyte life cycle hypothesis." Clinical Science 110, no. 1 (December 12, 2005): 1–9. http://dx.doi.org/10.1042/cs20050110.

Full text

Abstract:

The adipocyte life cycle hypothesis states that the metabolic properties of an adipocyte vary predictably during its life cycle: that as an adipocyte matures, it accumulates triacylglycerol (triglyceride) and becomes larger; that the rates of triacylglycerol synthesis and lipolysis are matched within adipocytes and that larger adipocytes, in general, have greater rates of triacylglycerol synthesis and, concurrently, greater rates of lipolysis and, therefore, larger adipocytes have greater rates of transmembrane fatty acid flux; and that the secretion of cytokines can also be related to adipocyte size with larger adipocytes having a more unfavourable profile of cytokine secretion than smaller adipocytes. Adipocyte location is an important modifier of this relationship and the favoured sites of adipocyte proliferation are a function of gender and the position within the life cycle of the organism at which proliferation occurs. The adipocyte life cycle hypothesis posits that the metabolic consequences of obesity depend on whether expansion of adipose tissue is achieved primarily by an increase in adipocyte number or adipocyte size. This hypothesis may explain a variety of previously unanswered clinical puzzles such as the vulnerability of many peoples from South East Asia to the adverse metabolic consequences of obesity.

APA, Harvard, Vancouver, ISO, and other styles

5

Mattacks, Christine A., and Caroline M. Pond. "The effects of dietary restriction and exercise on the volume of adipocytes in two intra-orbital depots in the guinea-pig." British Journal of Nutrition 53, no. 2 (March 1985): 207–13. http://dx.doi.org/10.1079/bjn19850028.

Full text

Abstract:

1. The volume of adipocytes in two intra-orbital sites and fourteen superficial and intra-abdominal sites, and the total adipocyte complement have been measured in virgin and reproductive guinea-pigs maintained on several different regimens of diet and exercise.2. The adipocytes around the ocular muscles at the back of the orbit (peripheral fat) are always larger than those just behind the eyeball (orbital fat).3. The adipocytes in both the intra-orbital sites are significantly larger in guinea-pigs whose total adipocyte complement is smaller than one standard deviation from the mean, than in those which have a normal-size or large adipocyte complement.4. The volume of intra-orbital adipocytes correlates very significantly with the volume of adipocytes in superficial and intra-abdominal sites in guinea-pigs which have large adipocyte complements, correlates weakly in those with normal adipocyte complements and not at all in those with small adipocyte complements.5. It is suggested that there may be fewer intra-orbital adipocytes in animals which have small adipocyte complements, and that, because the intra-orbital adipose tissue occupies a constant volume, the adipocytes in these sites become larger when they are less numerous.

APA, Harvard, Vancouver, ISO, and other styles

6

Naveiras, Olaia, Valentina Nardi, Parul Sharma, Peter Hauschka, and George Q. Daley. "Bone Marrow Adipocytes: A Novel Negative Regulator of the Hematopoietic Microenvironment." Blood 110, no. 11 (November 16, 2007): 1405. http://dx.doi.org/10.1182/blood.v110.11.1405.1405.

Full text

Abstract:

Abstract In the bone marrow (BM), osteoblasts and endothelium constitute functional niches providing positive or negative signals for hematopoietic stem cell (HSC) self-renewal. In addition to hematopoietic cells, endothelial cells, and osteoblasts, adult BM contains numerous adipocytes. Interestingly, the number of adipocytes correlates inversely with the gross hematopoietic activity of the marrow. Whether adipocytes have a direct effect on hematopoietic progenitors or whether they act as mere space-fillers in this context remains unclear. To determine the potential role of bone marrow adipocytes in hematopoiesis, we induced bone marrow-derived OP9 mesenchymal cells to differentiate into either osteoblastic or adipocytic stroma, and then tested their capacity to serve as surrogate HSC niches during in vitro hematopoietic culture in the absence of exogenous growth factors. We found that the presence of BM-derived adipocytes suppresses the expansion of short-term hematopoietic progenitors by at least two fold, as measured by the number of CD45+ cells expanded, the number of colony forming unit cells (CFU-Cs) and the competitive repopulation units (CRUs) during the first two months post-transplant. As an in vivo correlate, we compared the hematopoietic activity within the BM of the adipocyte-poor thoracic vertebrae and the adipocyte-rich proximal tail vertebrae. Indeed, we found that the percentage of HSCs (ckit+Lin-Sca1+), CMPs, GMPs and MEPs was decreased by two fold in the adipocyte-rich BM as determined phenotypically by FACS and functionally by short-term and long-term competitive repopulation assays. Mechanistically, oligonucleotide expression microarrays and conditioned media experiments on the OP9 co-cultures suggest that the inhibition of the progenitor compartment in adipocyte-rich environments is due to the loss of supportive factors (Notch ligands, N-cadherin, Angiopoietin-1, SCF, BMPs and Wnt5a) in addition to the presence of an active inhibitor. Finally, we found bone marrow adipocytes to accumulate in great numbers upon bone marrow ablation, a process that is hindered in genetically adipocyte-deficient mice. Since early BM transplant survival depends on the rapid accumulation of short term hematopoietic progenitors, whose replication we found hindered in adipocyte-rich BM, we were interested to explore whether the absence of adipocytes in the context of BM transplantation would foster faster recovery of lethally irradiated mice. As predicted, circulating leukocyte counts on the third week post-transplant were 3–5 times higher on the recovering fatless mice. Accordingly, the percentage of CFU-Cs, HSCs, CMPs, GMPs and MEPs on day 17 post-transplant was doubled on the adipocyte-depleted mice as compared to their wildtype littermates. We therefore conclude that, as seen in vitro, the presence of adipocytes in the recovering HSC niche is detrimental to the rapid hematopoietic expansion required to reconstitute blood production. We are currently examining the pharmacologic modulation of adipocyte formation for its effects in BM transplantation.

APA, Harvard, Vancouver, ISO, and other styles

7

Trotter, Timothy N., Tshering D. Lama-Sherpa, Deniz Peker, Amjad Javed, Larry J. Suva, and Yang Yang. "The Role of Adipocyte Lineage Cells in Myeloma Growth and Dissemination in Bone." Blood 126, no. 23 (December 3, 2015): 1797. http://dx.doi.org/10.1182/blood.v126.23.1797.1797.

Full text

Abstract:

Abstract Background: Multiple myeloma (MM) is hematologic malignancy of plasma cells that thrives in and progresses throughout the bone marrow microenvironment. The bone marrow is host to a variety of cell types, including bone marrow stromal cells and hematopoietic cells, as well as osteoblasts, osteoclasts and adipocytes. We and others have shown that MM cells not only alter the local bone microenvironment to support MM progression, but also modify distant bone sites through secretion of soluble factors before arrival of tumor cells. One critical alteration in bone is the shift of osteoblast progenitor cells from osteoblastogenesis towards adipogenesis. Whether and how these increased adipocyte lineage cells contribute to MM cells homing to and growth in bone are currently unknown. Both mature and pre-adipocytes have multiple endocrine functions such as cytokine and growth factor secretion. Thus, an increase in adipocyte lineage cells likely alters the bone microenvironment in favor of supporting MM. Here, we hypothesized that adipocytes and their precursors play an active role in MM progression that contributes to MM growth and dissemination throughout bone. Methods: Our hypothesis was tested using a co-culture system in which 3T3-L1 mouse pre-adipocytes or mature adipocytes were separated by a porous membrane from 5TGM1-luc mouse MM cells. This system allowed cross-talk by secreted molecules but not through direct cell-cell contact. After three days of co-culture, MM cells were collected for (i) intravenous (I.V.) tail-vein injections into syngeneic C57Bl/KaLwRiJ mice or (ii) protein collection for Western blot analyses. For in vivo experiments, tumor progression was tracked by bioluminescent luciferase imaging and total tumor burden was evaluated by IgG2bκ (a soluble marker of 5TGM1-luc MM cells) levels in mouse serum. In addition, conditioned medium (CM) was collected from either pre-adipocytes or mature adipocytes for MM cell migration assays or for analyses of soluble factors in the CM by cytokine/chemokine array. Results: I.V. injection of 5TGM1-luc MM cells into mice revealed that those previously co-cultured with pre-adipocytes more rapidly homed to bone and grew larger tumors compared to 5TGM1-luc MM cells cultured alone, whereas the MM cells cultured with mature adipocytes showed no significant increase in either bone homing or growth. Analysis of pre-adipocyte and mature adipocyte CM by cytokine/chemokine arrays demonstrated that pre-adipocytes secrete significantly more HGF, MCP-1, OPN and SDF-1α compared to mature adipocytes. Migration assays in which pre-adipocyte or mature adipocyte CM was used as a chemoattractant indicated that MM cells migrate significantly more towards both pre-adipocyte and mature adipocyte CM than fresh media. However, the pre-adipocyte CM exhibited significantly more chemoattraction than mature adipocyte CM. Furthermore, addition of an MCP-1 or SDF-1α neutralizing antibody to both pre-adipocyte CM and mature adipocyte CM resulted in significantly reduced migration of MM cells. However, pre-adipocyte CM required higher concentrations of antibodies than mature adipocyte CM, indicating a higher concentration of MCP-1 and SDF-1α in pre-adipocyte CM. MM cells also exhibited a significant dose-dependent migration towards recombinant pre-adipocyte factor-1 (Pref-1), a marker of pre-adipocytes that is down-regulated during adipogenesis. Finally, Western blots revealed that co-culture of MM cells with pre-adipocytes resulted in activation of β-catenin signaling, which is important for cell proliferation, survival and motility, in MM cells. Conclusions: These data indicate that adipocyte lineage cells play active but differentiation-dependent roles in MM progression, likely via the secretion of soluble factors. Both pre-adipocytes and mature adipocytes directly attract MM cells by secreting chemoattractants such as MCP-1 and SDF-1α. Interestingly, our data identify pre-adipocytes, and not mature adipocytes, as the main driver of the aggressive bone phenotype of MM cells. In sum, these data suggest that an increase in adipocyte lineage cells in the bone marrow at distant bone sites could feed back to MM cells and support MM dissemination to these distant bone sites. Studies to determine the intricacies of this novel role of pre-adipocytes in MM are currently ongoing. Disclosures Suva: University of Arkansas for Medical Sciences: Employment.

APA, Harvard, Vancouver, ISO, and other styles

8

Monji, Akio, Yang Zhang, G. V. Naveen Kumar, Christelle Guillermier, Soomin Kim, Benjamin Olenchock, and Matthew L. Steinhauser. "A Cycle of Inflammatory Adipocyte Death and Regeneration in Murine Adipose Tissue." Diabetes 71, no. 3 (January 18, 2022): 412–23. http://dx.doi.org/10.2337/db20-1306.

Full text

Abstract:

Adipose tissue (AT) expands by a combination of two fundamental cellular mechanisms: hypertrophic growth of existing adipocytes or through generation of new adipocytes, also known as hyperplastic growth. Multiple lines of evidence suggest a limited capacity for hyperplastic growth of AT in adulthood and that adipocyte number is relatively stable, even with fluctuations in AT mass. If the adipocyte number is stable in adulthood, despite well-documented birth and death of adipocytes, then this would suggest that birth may be coupled to death in a regenerative cycle. To test this hypothesis, we examined the dynamics of birth of new fat cells in relationship to adipocyte death by using high-fidelity stable isotope tracer methods in C57Bl6 mice. We discovered birth of new adipocytes at higher frequency in histological proximity to dead adipocytes. In diet-induced obesity, adipogenesis surged after an adipocyte death peak beyond 8 weeks of high-fat feeding. Through transcriptional analyses of AT and fractionated adipocytes, we found that the dominant cell death signals were inflammasome related. Proinflammatory signals were particularly evident in hypertrophied adipocytes or with deletion of a constitutive oxygen sensor and inhibitor of hypoxia-inducible factor, Egln1. We leveraged the potential role for the inflammasome in adipocyte death to test the adipocyte death-birth hypothesis, finding that caspase 1 loss of function attenuated adipocyte death and birth in murine visceral AT. These data collectively point to a regenerative cycle of adipocyte death and birth as a driver of adipogenesis in adult murine AT.

APA, Harvard, Vancouver, ISO, and other styles

9

Huang, Zhi Hua, DeSheng Gu, and Theodore Mazzone. "Role of adipocyte-derived apoE in modulating adipocyte size, lipid metabolism, and gene expression in vivo." American Journal of Physiology-Endocrinology and Metabolism 296, no. 5 (May 2009): E1110—E1119. http://dx.doi.org/10.1152/ajpendo.90964.2008.

Full text

Abstract:

Adipocytes isolated from apolipoprotein E (apoE)-knockout (EKO) mice display alterations in triglyceride (TG) metabolism and gene expression. The present studies were undertaken to evaluate the impact of endogenously produced adipocyte apoE on these adipocyte parameters in vivo, independent of the profoundly disturbed metabolic milieu of EKO mice. Adipose tissue from wild-type (WT) or EKO mice was transplanted into WT recipients, which were then fed chow or high-fat diet for 8–10 wk. After a chow diet, freshly isolated transplanted EKO adipocytes were significantly ( P < 0.05) smaller (70%) than transplanted WT adipocytes and displayed significantly lower rates of TG synthesis and higher rates of TG hydrolysis. Transplanted EKO adipocytes also had higher mRNA levels for adiponectin, perilipin, and genes coding for enzymes in the fatty acid oxidation pathway and lower levels of caveolin. After a high-fat diet and consequent increase in circulating lipid and apoE levels, transplanted WT adipocyte size increased by 106 × 103 μm3, whereas EKO adipocyte size increased only by 19 × 103 μm3. Endogenous host adipose tissue harvested from WT recipients of transplanted WT or EKO adipose tissue did not demonstrate any difference in adipocyte size. Consistent with the in vivo observations, EKO adipocytes synthesized less TG when incubated with apoE-containing TG-rich lipoproteins than WT adipocytes. Our results establish a novel in vivo role for endogenously produced apoE, distinct from circulating apoE, in modulation of adipocyte TG metabolism and gene expression. They support a model in which endogenously produced adipocyte apoE facilitates adipocyte lipid acquisition from circulating TG-rich lipoproteins.

APA, Harvard, Vancouver, ISO, and other styles

10

Münzberg, Heike, Elizabeth Floyd, and Ji Suk Chang. "Sympathetic Innervation of White Adipose Tissue: to Beige or Not to Beige?" Physiology 36, no. 4 (July 1, 2021): 246–55. http://dx.doi.org/10.1152/physiol.00038.2020.

Full text

Abstract:

Obesity research progresses in understanding neuronal circuits and adipocyte biology to regulate metabolism. However, the interface of neuro-adipocyte interaction is less studied. We summarize the current knowledge of adipose tissue innervation and interaction with adipocytes and emphasize adipocyte transitions from white to brown adipocytes and vice versa. We further highlight emerging concepts for the differential neuronal regulation of brown/beige versus white adipocyte and the interdependence of both for metabolic regulation.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Adipocyte"

1

Berry, Daniel C. "Retinoic acid in adipocyte biology." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1307733776.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Haynes, Kaylie. "Biochemical profiling of adipocyte metabolism." Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/10113/.

Full text

Abstract:

Obesity is a worldwide health issue that has reached epidemic proportions, and is defined as increased white adipose tissue mass. This increase in adiposity is caused by either hypertrophy of existing mature adipocytes, or hyperplasia of pre-adipocytes, leading to increased adipocyte numbers. The current study used the murine 3T3-L1 pre-adipocyte cell line to explore in vitro the differentiation process from pre-adipocytes to mature adipocytes, termed adipogenesis. Lipidomic analyses demonstrated a shift in the predominant lipid species present; from phospholipids in the pre-adipocytes, to triglycerides in the mature adipocytes. This was expected from the morphological changes known to occur in this cell line, from fibroblastic pre-adipocytes, to spherical lipid-loaded mature adipocytes. The production of various eicosanoids was also investigated, and their concentration was greatest during the pre-adipocyte stage. This profile was also seen with arachidonic acid, a precursor in eicosanoid synthesis. These changes in lipid metabolism and eicosanoid production appeared to be linked, allowing the differentiation process and lipid accumulation to continue. The obese state is also associated with a chronic low-grade inflammation, and so the effects of TNF-α and IL-6 intervention on adipocyte metabolism were investigated. Differences in lipid mobilisation caused by these pro-inflammatory agents were suggested due to increases or decreases observed in the concentrations of various triglyceride and fatty acid species. Increases were observed in the concentration of various detected eicosanoid species from the arachidonic acid cascade, mainly prostanoid species. Effects of the anti-inflammatory agent dexamethasone were also investigated in mature 3T3-L1 adipocytes. It was associated with increases in the concentration of both triglyceride and fatty acid species, suggesting possible increase in lipogenesis and/or decrease in lipolysis. Increases in the production of various eicosanoid species from the arachidonic acid pathway were also observed. The majority of these species are pro-inflammatory; however, PGE2 is known to have both pro-and anti-inflammatory effects, and this may help to explain these findings. In conclusion, the work presented in this thesis has revealed how adipocyte metabolism changes in the naturally occurring stages of adipogenesis, as well as in response to pro- and anti-inflammatory intervention. Associations were observed between adipokine gene expression, lipid metabolism and eicosanoid production; however, further work is required to confirm these links by identifying the underlying mechanisms involved.

APA, Harvard, Vancouver, ISO, and other styles

3

Wang, Ping. "Proteomic, transcriptomic and epidemiological analysis of adipocyte-secreted proteins towards a system biological understanding of adipocytes /." Maastricht : Maastricht : Universitaire Pers ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=13845.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Eriksson, Maria. "Adipocyte-derived hormones and cardiovascular disease." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36679.

Full text

Abstract:

Obesity is increasing globally and related to major changes in lifestyle. This increase is associated with an increased risk of cardiovascular disease (CVD). Knowledge about adipose tissue as a metabolic-endocrine organ has increased during the last few decades. Adipose tissue produces a number of proteins with increased body weight, many of which are important for food intake and satiety, insulin sensitivity, and vessel integrity, and aberrations have been related to atherosclerosis. Notably, the risk for developing CVD over the course of a lifetime differs between men and women. In Northern Sweden, men have a higher risk for myocardial infarction (MI). However, the incidence is declining in men but not in women. These sex differences could be due to functional and anatomical differences in the fat mass and its functions. The primary aim of this thesis was to evaluate associations between the adipocyte-derived hormones leptin and adiponectin, and fibrinolysis and other variables associated with the metabolic syndrome, and particularly whether these associations differ between men and women. Another aim was to evaluate these associations during physical exercise and pharmacological intervention (i.e. enalapril). Finally, whether leptin and adiponectin predict a first MI or sudden cardiac death with putative sex differences was also investigated. The first study used a cross-sectional design and included 72 men and women recruited from the WHO MONICA project. We found pronounced sex differences in the associations with fibrinolytic variables. Leptin was associated with fibrinolytic factors in men, whereas insulin resistance was strongly associated with all fibrinolytic factors in women. The second study was an experimental observational study with 20 men exposed to strenuous physical exercise. During exercise, leptin levels decreased and adiponectin levels increased, and both were strongly associated with an improved fibrinolytic capacity measured as decreased PAI-1 activity. Changes in insulin sensitivity were not associated with changing adiponectin levels. The third study was a randomised, double-blind, single centre clinical trial including 46 men and 37 women who had an earlier MI. The study duration was one year, and participating subjects were randomised to either placebo or ACE inhibitor (i.e. enalapril). Circulating leptin levels were not associated with enalapril treatment. During the one-year study, changes in leptin levels were associated with changes in circulating levels of tPA mass, PAI-1 mass, and tPA-PAI complex in men, but not vWF. These associations were found in all men and men on placebo treatment. In women on enalapril treatment there was an association between changes in leptin and changes in vWF. In the fourth study, the impact of leptin, adiponectin, and their ratio on future MI risk or sudden cardiac death was tested in a prospective nested casecontrol study within the framework of the WHO MONICA, Västerbotten Intervention Project (VIP), and Västerbotten Mammary Screening Program (MSP). A total 564 cases (first-ever MI or sudden cardiac death) and 1082 matched controls were selected. High leptin, low adiponectin, and a high leptin/adiponectin ratio independently predicted a first-ever MI, possibly with higher risk in men in regards to leptin. The association was found for non-fatal cases with ST-elevation MI. Subjects with low adiponectin levels had their MI earlier than those with high levels. In conclusion, the adipocyte-derived hormones leptin and adiponectin are related to the development of CVD with a sex difference, and fibrinolytic mechanisms could be possible contributors to CVD risk.

APA, Harvard, Vancouver, ISO, and other styles

5

Constant, Vanessa Auguste. "Macrophage-conditioned medium inhibits adipocyte differentiation." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27967.

Full text

Abstract:

Obesity is accompanied by a reduced adipogenic capacity that promotes a dipocyte hypertrophy, low-grade inflammation, and insulin resistance. Macrophages infiltrate adipose tissue and may contribute to the low-grade inflammation associated with obesity and insulin resistance, suggesting that they could also play an anti-adipogenic role. I hypothesized that macrophage-secreted factors inhibit adipogenesis. My objectives were to assess if macrophage-conditioned medium (MacCM) inhibits adipocyte differentiation and to determine the mechanism by which the inhibition occurs. Murine J774 or human THP-1 MacCM was added to murine 3T3-L1 or human abdominal subcutaneous or omental preadipocytes. Either type of MacCM impaired murine and human adipogenesis as measured by triglyceride accumulation and protein expression of adipogenic markers. Time course studies revealed that THP-1-MacCM was required during the early phase of 3T3-L1 adipogenesis for its inhibitory effect. THP-1-MacCM stimulated the phosphorylation of ERK1/2 and IKKbeta in 3T3-L1 preadipocytes. Pharmacological inhibition of ERK1/2, with the specific MEK1 inhibitor PD98059, alleviated the inhibitory effect of THP-1-MacCM on TG accumulation. In conclusion, MacCM inhibits adipocyte differentiation in culture. The antiadipogenic effect depends on early exposure of THP-1-MacM to differentiating 3T3-L1 preadipocytes, and ERK1/2 is required for the inhibitory effect of THP-1-MacCM on TG accumulation.

APA, Harvard, Vancouver, ISO, and other styles

6

Hubber, Naomi Annette. "Sensing and control of adipocyte function." Thesis, Aston University, 2006. http://publications.aston.ac.uk/15327/.

Full text

Abstract:

This thesis has investigated adipocytes development and adipokine signalling with a view to enhance the understanding of tissue functionality and to identify possible targets or pathways for therapeutic intervention. Adipocyte isolation from human tissue samples was undertaken for these investigative studies, and the methodology was optimised. The resulting isolates of pre-adipocytes and mature adipocytes were characterised and evaluated. Major findings from these studies indicate that mature adipocytes undergo cell division post terminal differentiation. Gene studies indicated that subcutaneous adipose tissue exuded greater concentrations and fluctuations of adipokine levels than visceral adipose tissue, indicating an important adiposensing role of subcutaneous adipose tissue. It was subsequently postulated that the subcutaneous depot may provide the major focus for control of overall energy balance and by extension weight control. One potential therapeutic target, 11β-hydrosteroid dehydrogenase (11β-HSD1) was investigated, and prospective inhibitors of its action were considered (BVT1, BVT2 and AZ121). Selective reduction of adiposity of the visceral depot was desired due to its correlation with the detrimental effects of obesity. However, studies indicated that although the visceral depot tissue was not unaffected, the subcutaneous depot was more susceptible to therapeutic inhibition by these compounds. This was determined to be a potentially valuable therapeutic intervention in light of previous postulations regarding long-term energy control via the subcutaneous tissue depot.

APA, Harvard, Vancouver, ISO, and other styles

7

Hopf, Lisa-Marie. "Regulation von Adipocyte fatty acid binding protein in Abhängigkeit der Nierenfunktion." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-197266.

Full text

Abstract:

Adipositas und die damit verbundenen Folgeerkrankungen sind eine der zentralen Gesund-heitsherausforderungen unserer Zeit. Dauerhafte Adipositas führt zu einer Dysregulation fettgewebseigener Peptidhormone. Diese sogenannten Adipokine stellen ein Verbindungsglied zwischen Fettgewebsakkumulation und den vielfältigen Adipositaskomplikationen des gesamten Organismus dar. Adipocyte fatty acid binding protein (AFABP) wurde in den letzten Jahren als zirkulierendes Adipokin mit diabetogenen, proinflammatorischen und proateriosklerotischen Effekten etabliert. Zu Beginn der Dissertation lagen unzureichende Erkenntnisse über die Elimination von AFABP sowie die Regulation des Adipokins bei eingeschränkter Nierenfunktion vor. Aus diesem Grund untersucht die vorliegende Arbeit die AFABP-Regulation in Abhängigkeit von der Nierenfunktion in 532 Patienten mit chronischer Niereninsuffizienz (Studienpopulation 1) und 32 Patienten mit akuter Nierenfunktionsverminderung nach Nephrektomie (Studienpopulation 2). In beiden Kohorten stiegen die medianen AFABP-Serumkonzentrationen mit abfallender Nierenfunktion an. Zudem waren Marker der Nierenfunktion in beiden Studienpopulationen die stärksten unabhängigen Prädiktoren für zirkulierendes AFABP. Untersuchungen aus der Arbeitsgruppe zur AFABP-Regulation in einem Rattenmodell der akuten Niereninsuffizienz unterstützen die klinischen Studienergebnisse. Zusammenfassend zeigen diese Ergebnisse zum ersten Mal signifikant steigende AFABP-Serumspiegel bei chronischer und akuter Nierenfunktionsstörung, sowie bei akutem Abfall der Nierenfunktion. Diese Befunde stützen die Hypothese, dass AFABP renal eliminiert wird. Inwiefern AFABP darüber hinaus in die Pathogenese der chronischen Niereninsuffizienz eingreift, muss in weiterführenden Studien beleuchtet werden.

APA, Harvard, Vancouver, ISO, and other styles

8

Tong, Xiaohui. "Rôle de la synthèse des miARN par le tissu adipeux dans les pathologies de vieillissement." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30332.

Full text

Abstract:

Au cours du vieillissement, le tissu adipeux devient sénescent ce qui conduit à une altération des capacités fonctionnelles de l'adipocyte. En effet, la senescence est un arrêt du cycle cellulaire qui entraîne la perte de fonction et entretient un profil inflammatoire. Ces changements participent à l'installation progressive de pathologies associées au vieillissement comme le diabète, l'athérosclérose ou les maladies neurodégénératives. Afin de mieux comprendre le rôle des sécrétions de l'adipocyte dans la perte de fonction de cette cellule, nous avons analysé la production de micro ARNs de l'adipocyte âgé chez la souris. Depuis plusieurs années, l'étude des micros ARNs montre que ces molécules pourraient devenir des cibles thérapeutiques de premier plan ou des biomarqueurs spécifiques. Dans ce contexte, nous avons analysé et caractérisé le MiRnome de l'adipocyte chez la souris âgée et nous avons pu démontrer que le Mir-1949 pouvait jouer un rôle important dans la perte de fonction de l'adipocyte au cours du vieillissement. En effet, l'expression et la sécrétion adipocytaire de mir- 1949 sont augmentées avec l'âge et semblent être associées à l'état de senescence de la cellule adipeuse. De plus, l'augmentation de mir-1949 provoque une altération des fonctions de l'adipocyte in vitro. L'ensemble de ces résultats préliminaires montre que mir-1949 pourrait devenir une adipokine d'intérêt à cibler au cours du vieillissement
On the one part, dicer, the RNase III endoribonuclease responsible for microRNAs maturation, has been reported to be decreased in adipocytes during ageing. With the use of tamoxifen inducible dicerlox/lox/ adiponectin-CreERT2 mice, we found that adipocyte dicer deficiency promoted the onset of some of the age-related complications such as reduced adipocyte sizes and dysfunctions in systemic metabolism. The abrogation of white adipocyte markers such as Pparγ, Glut4 or Hsl, indicated that dicer is indispensible for the maintainance of white adipocyte identity. In addition, the results that there were lipid accumulation and fibrosis in liver in tamoxifen treated dicerlox/lox/ adiponectin-CreERT2+ mice, indicated that adipocyte dicer deficiency might contribute to liver aging. Mechanistically, mitochondrial function seemed to be upregulated due to adipocyte dicer deficiency, indicated by increased protein levels of OXPHOS components and PGC1α. In line, mitochondria repressors FOXO1 and FOXO3 were phosphorylated and inactivated, whose downstream antioxidant targets Catalase and Sod were also decreased. Moreover, P16, a marker of senescence, exhibited a trend to be increased due to adipocyte dicer deficiency. Since mitochondrial ROS surplus can lead to DNA damage and senescence, we assured that adipocyte dicer deficiency might induce a combination of mitochondrial activation and reduction in detoxification reduction possibly mediated by the inactivation of FOXO1 and FOXO3a. Finally, the result that nutrient restriction positively regulated dicer level in adipocytes further supported that there is a conserved aging pathway in adipocytes involving dicer. On the other part, through microarray screen and RT-qPCR validation, we reported that aging increased mir-1949 in adipocytes in wild type mice and possibly promoted its secretion from perigonadal adipose tissue in vitro. Correspondingly, in vitro results also suggested that senescence increased mir-1949 production and secretion from adipocytes. Functionally, upregulation of mir-1949 in 3T3-F442A adipocytes negatively regulated mitochondrial complex II protein level and oxygen consumption capability, associated with lipid accumulation. Interestingly, sustained upregulation of mir-1949 during adipogenesis of 3T3-F442A preadipocytes, tended to increase white adipocyte markers, such as Leptin, Glut4 or Hsl. Finally, combined with the results that 24h fasting significantly increased mir-1949 in perigonadal adipose tissue as well as that upregulation of mir-1949 exhibited a trend to increase lipid accumulation in senescent 3T3-F442A adipocytes, we assured that aging increases mir-1949 expression in adipocytes which might try to rescue age-related dysfunctions in adipocytes, such as impaired lipid storage. Nevertheless, the precise actions of mir-1949 need to be validated in vivo by injection of AAV-aP2-mir-1949 mimic into aged mice

APA, Harvard, Vancouver, ISO, and other styles

9

Hussain, Abid. "Impact of LYL1 deficiency on adipocyte differentiation." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS061.

Full text

Abstract:

LYL1 (Lymphoblastic leukemia-derived sequence 1) est un facteur de transcription basic hélice-boucle-hélice (bHLH) exprimé dans les lymphocytes B, les cellules myéloïdes et les cellules endothéliales (CE). Les souris déficientes pour Lyl1 (Lyl1-/-) sont viables et chez la souris adulte, LYL1 a un rôle majeur dans la maturation des vaisseaux sanguins nouvellement formés et dans le contrôle de la perméabilité vasculaire basale, suggérant l'importance de LYL1 dans le maintien de la quiescence et/ou stabilisation des CE. Les vaisseaux sanguins représentent une barrière entre le sang et le tissu conjonctif. Ils peuvent également jouer le rôle de niche vasculaire contenant des progéniteurs des différentes cellules murines (par exemple, des cellules hématopoïétiques, des cellules β-pancréatiques, des cellules neuronales, des cellules hépatiques et des cellules adipeuses). Les deux tissus adipeux, blancs et bruns (WAT et BAT), sont très vascularisés. Jusqu'à présent, rien n'était connu sur le rôle de LYL1 dans le tissu adipeux. Les résultats présentés dans cette thèse montrent que l'augmentation significative du poids corporel des mâles Lyl1-/- par rapport aux souris sauvages (WT), sous régime normal, n'est pas associée à des troubles métaboliques. Ils présentent également un poids plus élevé de tissus adipeux (WAT et BAT) et de plus grandes gouttelettes lipidiques. In vivo, la perte de Lyl1 accélère le processus de différenciation des cellules souches adipeuses (CSA), puisque les adipocytes blancs et bruns sont matures et actifs plus tôt. De plus, les CSA sont moins nombreuses dans les tissus adipeux, ce qui confirme que la perte de Lyl1 favorise la différenciation des CSA vers adipocytes matures. Nous avons également démontré que Lyl1 est exprimée dans les CSA et les pré-adipocytes, suggérant un rôle direct dans LYL1 dans la différenciation adipocytaire. D'autre part, les vaisseaux des WAT des souris Lyl1-/- sont mal recouverts de cellules murales et plus perméables, suggérant que la niche vasculaire des tissus adipeux pourrait être perturbée. Sous alimentation riche en graisses (HFD), le poids corporel et le poids du tissu adipeux sont plus faibles chez les souris Lyl1-/- par rapport à WT. De plus les souris Lyl1-/- présentent de plus petites gouttelettes lipidiques que les WT, sous HFD. Ces résultats préliminaires, suggèrent que les souris Lyl1-/- pourraient être protégées contre l'obésité induite par l'alimentation. Cependant d'autres expériences sont nécessaires pour valider ces résultats. Il existe probablement un mécanisme de compensation qui se met en place chez les souris Lyl1-/- sous HFD. Ce travail a démontré que, sans Lyl1, la différenciation adipocytaire est accélérée et que la niche vasculaire adipocytaire est perturbée
LYL1 (Lymphoblastic leukemia-derived sequence 1) is a basic helix-loop-helix (bHLH) transcriptional factor, which is expressed in B lymphocytes, myeloid cells and endothelial cells (EC). Lyl1 deficient (Lyl1-/-) mice are viable and in adult mice, LYL1 has an active role in the maturation of newly formed blood vessels and is also involved in the control of basal vascular permeability, suggesting that LYL1 is required for the maintenance of EC quiescence and stabilization. Blood vessels provide a barrier between connective tissue and blood. They also have been described as “vascular niche” containing progenitors of different murine cells (e.g. hematopoietic cells, pancreatic β-cells, neuronal cells, liver cells and adipose cells). Both white and brown adipose tissues (WAT and BAT) are highly vascularized. Up to now, nothing was known concerning the role of LYL1 in adipose tissue. The results presented in this thesis revealed that the significant increase in body weight of Lyl1-/- males compared to their wild type (WT) littermates under chow diet is not due to any metabolic disorders. They also showed higher adipose tissue weights (BAT and WAT) and bigger lipid droplets. In vivo Lyl1 deficiency cause early differentiation process of adipose stem cells (ASCs) since both white and brown adipocytes are mature and active faster. In addition, ASCs are less numerous in Lyl1-/- adipose tissues, which confirm that Lyl1 deficiency favors the differentiation of ASCs towards mature adipocytes. We also demonstrated that Lyl1 is expressed both in ASCs and pre-adipocytes, suggesting a direct role of LYL1 in adipocyte differentiation. On the other hand, the vessels in Lyl1-/- WAT are poorly covered with mural cells and more permeable, proposing that adipose stem cell vascular niche could be disturbed. Under high fat diet (HFD), total body weight and adipose tissue weight are lower in Lyl1-/- mice compared to WT. Moreover smaller lipid droplets were observed in Lyl1-/- mice under HFD. These preliminary results suggest that Lyl1-/- mice could be protected from diet-induced obesity. However more experiments are needed to validate these results. Probably there is a compensatory type of mechanism going on under HFD in Lyl1-/- mice. This work demonstrated that under Lyl1 deficiency adipocyte differentiation process becomes faster and adipose tissue vascular niche could be disturbed

APA, Harvard, Vancouver, ISO, and other styles

10

Pulbutr, Pawitra. "Roles of Calcium in Adipocyte Cell Function." Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508248.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Adipocyte"

1

Steenbock Symposium (27th 1999 Madison, Wis.). Adipocyte biology and hormone signaling. Amsterdam, The Netherlands: IOS Press, 2000.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

2

J, Hausman Gary, and Martin Roy J, eds. Biology of the adipocyte: Research approaches. New York: Van Nostrand Reinhold, 1987.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Cheng, Anita Yuen Man. The biochemistry ans molecular biology of human adipocyte reversion. Ottawa: National Library of Canada, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Ha, Elizabeth. Adipocyte-specific Tribbles-1 Regulates Plasma Adiponectin and Lipoprotein Metabolism in Mice. [New York, N.Y.?]: [publisher not identified], 2021.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

5

Martin-Carli, Jayne Frances. RPGRIP1L and FTO – genes implicated in the effects of FTO intronic sequence variants on food intake – also affect adipogenesis and adipocyte biology. [New York, N.Y.?]: [publisher not identified], 2017.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

6

Weber, Michelle J., and John M. Hoffmann. Adipocytes: Biology, regulation and health impact. Hauppauge, N.Y: Nova Science Publishers, 2012.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

7

Sciot, Raf, Clara Gerosa, and Gavino Faa, eds. Adipocytic, Vascular and Skeletal Muscle Tumors. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-37460-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Adipocytes Secrete Lipid-Laden Exosomes and Influence Local Macrophage Behavior. [New York, N.Y.?]: [publisher not identified], 2020.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

9

Cho, Charles Young. Role of oxidative stress in two models of insulin resistance within primary rat adipocytes. Ottawa: National Library of Canada, 1999.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

10

A, Bray George, Ryan Donna H, and Pennington Biomedical Research Center, eds. Nutrition, genetics, and obesity. Baton Rouge: Louisiana State University Press, 1999.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "Adipocyte"

1

Moreno-Navarrete, José María, and José Manuel Fernández-Real. "Adipocyte Differentiation." In Adipose Tissue Biology, 17–38. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0965-6_2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Phung, Thuy L., Teresa S. Wright, Crystal Y. Pourciau, and Bruce R. Smoller. "Adipocyte Proliferations." In Pediatric Dermatopathology, 567–72. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44824-4_27.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Christofides, Elena A. "The Adipocyte." In Bariatric Endocrinology, 19–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95655-8_2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Moreno-Navarrete, José María, and José Manuel Fernández-Real. "Adipocyte Differentiation." In Adipose Tissue Biology, 69–90. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52031-5_3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Rayalam, Srujana, and Clifton A. Baile. "Adipocyte Growth and Factors Influencing Adipocyte Life Cycle." In Adipose Tissue Biology, 195–226. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0965-6_7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Carrageta, David F., Pedro F. Oliveira, Mariana P. Monteiro, and Marco G. Alves. "Adipocyte Specific Signaling." In Tissue-Specific Cell Signaling, 409–36. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44436-5_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Schulz, Carla, Kerstin Paulus, and Hendrik Lehnert. "Adipocyte–Brain: Crosstalk." In Results and Problems in Cell Differentiation, 189–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14426-4_16.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Dugail, Isabelle, and Soizic Le Lay. "Adipocyte Lipid Droplet Physiology." In Physiology and Physiopathology of Adipose Tissue, 123–39. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0343-2_9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Carey, Gale B. "Mechanisms Regulating Adipocyte Lipolysis." In Advances in Experimental Medicine and Biology, 157–70. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1928-1_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Tao, Zhipeng, Longhua Liu, Louise D. Zheng, and Zhiyong Cheng. "Autophagy in Adipocyte Differentiation." In Autophagy in Differentiation and Tissue Maintenance, 45–53. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7651_2017_65.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Adipocyte"

1

Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

Full text

Abstract:

Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells

APA, Harvard, Vancouver, ISO, and other styles

2

Liu, Fujun, Fuyong Xing, Hai Su, and Lin Yang. "Touching adipocyte cells decomposition using combinatorial optimization." In 2014 IEEE 11th International Symposium on Biomedical Imaging (ISBI 2014). IEEE, 2014. http://dx.doi.org/10.1109/isbi.2014.6868125.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Tucci, Jonathan, Xia Sheng, and Steven D. Mittelman. "Abstract 4339: Acute lymphoblastic leukemia cells stimulate adipocyte lipolysis and utilize adipocyte-derived free-fatty acids for proliferation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4339.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Kim, Jeong Hee, Zhenhui Liu, and Ishan Barman. "Deep learning-assisted 3D virtual staining for the study of adipogenesis." In Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/fio.2022.jtu7b.3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Phillips, E., T. Kleffmann, H. Morrin, B. Robinson, and M. Currie. "PO-307 Differential secretome analysis of cancer-associated adipocytes (CAA) and mature adipocytes to identify adipocyte-driven micro-environmental regulators of breast cancer progression." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.820.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Kumar, Sushil, Dileep Kumar, Komal Raina, Rajesh Agarwal, and Chapla Agarwal. "Abstract 4116: Grape seed extract impairs adipocyte-colorectal cancer cell interaction and decreases adipocyte-driven colon cancer stem colonosphere formation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4116.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Kim, Jong-Sang, Ji-Sun Lim, Annalene Garcia, Ji-Yeon Seo, Jia Park, Dae Hwan Nam, Mi Kyung Sung, and Young-Rok Seo. "Abstract 4579: Effect of pre-adipocyte and differentiated adipocyte conditioned media on galectin-3 expression in mouse intestinal epithelial cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4579.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

AlJaber, Dr Mashael Jamal, Amal Salem Bashraheel, DR Shen Lei, Dr Mostafa Abbas, Dr Moataz Bashah, Dr Morana Jajanjac, Afnan Almenhali, Dr Nelson Orie, Dr Vidya Mohamed-Ali, and Dr Aysha Bakhamis. "Hyperinsulinemia is associated with adipocyte hypertrophy and mitochondrial dysfunction." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2018. http://dx.doi.org/10.5339/qfarc.2018.hbpd1053.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Gohlke, S., F. Garcia-Carrizo, and TJ Schulz. "Role of mast cells in age-related brown adipocyte dysfunction." In Abstracts der Adipositastage 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1693609.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Mazloum, Nayef Ali. "Suppression of adipocyte hyperplasia through SIRT1mediated inhibition of cMyc function." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2018. http://dx.doi.org/10.5339/qfarc.2018.hbpp830.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Adipocyte"

1

Bulun, Berdar E. Adipocyte Differentiation: Relationship to Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2002. http://dx.doi.org/10.21236/ada405263.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Bulun, Serdar E. Adipocyte Differentiation: Relationship to Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391323.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Diaz-Meco, Maria T. Targeting the Adipocyte-Tumor Cell Interaction in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada610957.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Mizinga, Kemmy M. Promoter Switching and Transcription Factor Usage During Breast Adipocyte Differentiation: Role in Aromatase Expression and Activity. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada447636.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Mizinga, Kemmy M. Promoter Switching and Transcription Factor Usage During Breast Adipocyte Differentiation Role in Aromatase Expression and Activity. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada432079.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.

Full text

Abstract:

The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.

APA, Harvard, Vancouver, ISO, and other styles

7

Camarillo, Ignacio, and Maxine Nichols. Breast Cancer and Early Onset Childhood Obesity: Cell Specific Gene Expression in Mammary Epithelia and Adipocytes. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada483660.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!